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Physicians have long known that patients with an underactive thyroid tend to have anemia because thyroid hormone stimulates red blood cell (RBC) production.
Now, researchers say they have determined how this occurs.
Xiaofei Gao, PhD, of Westlake Institute for Advanced Study in Hangzhou, Zhejiang Province, China, and his colleagues conducted this research and reported the results in PNAS.
The team began by studying the formation of human RBCs in culture. They wondered if something in the culture serum was essential for RBC maturation. So they ran the serum through a charcoal filter, which attracts and retains hydrophobic molecules.
Once filtered, the serum no longer supported RBC production. This validated the researchers’ theory that one of the hydrophobic molecules was key to RBC maturation.
In fact, the team found thyroid hormone was essential for the final step of RBC maturation.
When the researchers added thyroid hormone back to the serum, RBC progenitors once again started down the path to maturation.
If thyroid hormone was added at an earlier stage of development, the RBCs short-circuited their usual developmental processes and began turning into mature RBCs.
With further investigation, the researchers pinpointed the receptor inside maturing RBCs to which thyroid hormone binds—thyroid hormone receptor beta (TRβ).
From there, the team found that nuclear receptor coactivator 4 (NCOA4), a protein necessary for thyroid hormone stimulation, works with TRβ to regulate RBC development.
Finally, experiments showed that TRβ agonists could stimulate RBC development and alleviate anemic symptoms in a mouse model of chronic anemia.
The researchers therefore believe this work could lead to new therapies for anemic patients, including those with an underactive thyroid. 
Physicians have long known that patients with an underactive thyroid tend to have anemia because thyroid hormone stimulates red blood cell (RBC) production.
Now, researchers say they have determined how this occurs.
Xiaofei Gao, PhD, of Westlake Institute for Advanced Study in Hangzhou, Zhejiang Province, China, and his colleagues conducted this research and reported the results in PNAS.
The team began by studying the formation of human RBCs in culture. They wondered if something in the culture serum was essential for RBC maturation. So they ran the serum through a charcoal filter, which attracts and retains hydrophobic molecules.
Once filtered, the serum no longer supported RBC production. This validated the researchers’ theory that one of the hydrophobic molecules was key to RBC maturation.
In fact, the team found thyroid hormone was essential for the final step of RBC maturation.
When the researchers added thyroid hormone back to the serum, RBC progenitors once again started down the path to maturation.
If thyroid hormone was added at an earlier stage of development, the RBCs short-circuited their usual developmental processes and began turning into mature RBCs.
With further investigation, the researchers pinpointed the receptor inside maturing RBCs to which thyroid hormone binds—thyroid hormone receptor beta (TRβ).
From there, the team found that nuclear receptor coactivator 4 (NCOA4), a protein necessary for thyroid hormone stimulation, works with TRβ to regulate RBC development.
Finally, experiments showed that TRβ agonists could stimulate RBC development and alleviate anemic symptoms in a mouse model of chronic anemia.
The researchers therefore believe this work could lead to new therapies for anemic patients, including those with an underactive thyroid.
Physicians have long known that patients with an underactive thyroid tend to have anemia because thyroid hormone stimulates red blood cell (RBC) production.
Now, researchers say they have determined how this occurs.
Xiaofei Gao, PhD, of Westlake Institute for Advanced Study in Hangzhou, Zhejiang Province, China, and his colleagues conducted this research and reported the results in PNAS.
The team began by studying the formation of human RBCs in culture. They wondered if something in the culture serum was essential for RBC maturation. So they ran the serum through a charcoal filter, which attracts and retains hydrophobic molecules.
Once filtered, the serum no longer supported RBC production. This validated the researchers’ theory that one of the hydrophobic molecules was key to RBC maturation.
In fact, the team found thyroid hormone was essential for the final step of RBC maturation.
When the researchers added thyroid hormone back to the serum, RBC progenitors once again started down the path to maturation.
If thyroid hormone was added at an earlier stage of development, the RBCs short-circuited their usual developmental processes and began turning into mature RBCs.
With further investigation, the researchers pinpointed the receptor inside maturing RBCs to which thyroid hormone binds—thyroid hormone receptor beta (TRβ).
From there, the team found that nuclear receptor coactivator 4 (NCOA4), a protein necessary for thyroid hormone stimulation, works with TRβ to regulate RBC development.
Finally, experiments showed that TRβ agonists could stimulate RBC development and alleviate anemic symptoms in a mouse model of chronic anemia.
The researchers therefore believe this work could lead to new therapies for anemic patients, including those with an underactive thyroid.